METABOLIC AND HORMONAL RESPONSES TO ADRENOCEPTOR ANTAGONISTS IN EXERCISING RATS

alpha- and beta-adrenoceptors play a key role in the regulation of nut rient supply to working muscles during exercise. To assess their influ ence in the regulation of substrate utilization, rats were studied dur ing alpha- or beta-adrenoceptor blockade. Energy metabolism was studie d by means of indirect calorimetry before, during, and after moderate swimming exercise. Blood samples were taken far the determination of n utrient and hormone concentrations. In addition, central venous blood samples were withdrawn for determination of blood gases, pH, and total hemoglobin concentration (c/Hb). alpha- and beta-adrenoceptor blockad e decreased the rates of energy expenditure (EE) and fat oxidation (fa t-ox) during and after swimming in comparison to swimming without adre noceptor blockade. The oxidation of carbohydrates (CHO-ox) was increas ed in both cases. alpha-Blockade prevented the exercise-induced increa se in blood glucose, plasma free fatty acids (FFA) were not affected, and plasma insulin, norepinephrine (NOR), epinephrine (EPI), and lacta te were markedly increased. beta-adrenoceptor blockade prevented the e xercise-induced increases in blood glucose and FFA. EPI increased slig htly more than and NOR less than in the control experiment. The exerci se-induced decrease in insulin was more pronounced after beta-blockade . alpha-Blockade caused a less pronounced decrease in venous oxygen sa turation (SO2) and tension (PO2) than in the control experiment. The e xercise-induced increase in carbon dioxide tension (PCO2) was almost a bsent. After beta-blockade, venous SO2 and PO2 decreased more and PCO2 increased more than in the control experiment. It is concluded that b oth alpha- and beta-blockade restrict the rate of EE during exercise. In the case of beta-blockade, this may be due to an insufficient suppl y of nutrients, mainly FFA, although the oxygen supply to the muscles also seems to be diminished by inhibition of the exercise-induced incr ease in cardiac output and prevention of beta-adrenergically mediated vasodilatation in working muscles. In the case of alpha-blockade, the restriction of energy metabolism seems mainly to be due to an insuffic ient supply of oxygen caused by prevention of redistribution of cardia c output mainly resulting from insufficient vasoconstriction in the vi sceral vascular bed. Copyright (C) 1995 by W.B. Saunders Company